To explore the role of percent free-prostate specific antigen(PSA) on the differentiation between benign and malignant prostatic diseases in patients with serum total PSA levels between 4.0 and 10.0 ng/ml. Forty-three out of the 221 screened men who had total PSA levels between 4.0 and 10.0 ng/ml were retrospectively enrolled into this study. in addition to digital rectal examination(DRE), transrectal ultrasonography(TRUS), and total PSA, they received either TRUS-guided biopsies(n=27) or transurethral resection of the prostate (TUR-P) (n=16). All sample sera were then stored at -70 °C after the initial measurement of total PSA levels using an immunoenzymometric assay(Tandem-E®, Hybritech). Thereafter, all stored sera were quantified for free-PSA levels and total PSA levels using a different radioimmunometric assay(PSA-RJACT, CIS). Two values of percent free-PSA were obtained for each individual by dividing the same free-PSA level by 2 different total PSA values as measured by 2 different assays. Among the 43 patients, there were 34(79.1%) patients with benign prostatic hyperpla-sia(BPH), 5(11.6%) with prostatitis, and 4(9.3%) with prostate cancer(PC). Using these 2 different total PSA assays, the percent free-PSA in patients with BPH, prostatitis, and PC were 28.0%±12.2%, 23.6%±9.1%, 8.7%±1.3% (FPSA-RJACT/Tandem-E®) and 29.6%±13.1%,28.5%±13.1%, 9.7%±1.1% (FPSA-RJACT/PSA-RIACT), respectively. Patients with PC had significantly lower values of percent free-PSA (less than 12%) while those with either BPH or prostatitis had values greater than l2%(p values, 0.015 and 0.003, unpaired t-test). In contrast, the percent free-PSA values were not statistically different between BPH and prostatitis patients in both assays (p=0. 44, unpaired t-test). Besides, the correlation between the 2 values of percent free-PSA was good(r2 =0.90), based on 2 different assays for total PSA levels. Our study implies that percent free-PSA can help differentiate prostate cancer from benign prostatic diseases, and thus greatly reducing unnecessary biopsies. There is no need to measure the total PSA levels again while determining the percent free-PSA.
Purpose: The human telomerase reverse transcriptase (hTERT) promoter is used to restrict adenoviral expression of suicide or proapoptotic genes in telomerase-positive cancer cells. Etoposide can enhance intratumoral transgene expression in mice immunized with adenoviral vectors. The aim of this study is to evaluate whether greater therapeutic benefit can be achieved by combination treatment of low-dose etoposide and replication-incompetent adenoviral vectors encoding cytosine deaminase (CD) driven by the hTERT promoter for murine bladder carcinoma.
<b><i>Purpose:</i></b> To investigate the association of prostate blood flow (PBF) with lower urinary tract symptoms (LUTS) in aged males using Doppler spectral waveform (DSW) analysis. <b><i>Patients and Methods:</i></b> We performed a prospective analysis involving 133 aged males with clinical diagnosis of LUTS. DSW parameters (peak-systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index (RI)) were measured at bilateral neurovascular bundles (NVB), periurethral, and capsular branches by Doppler transrectal ultrasound with the patient in the right lateral decubitus position. The associations of PBF parameters and the International Prostate Symptom Score (IPSS) were analyzed. <b><i>Results:</i></b> Overall, total IPSS scores were significantly correlated with the RI of bilateral NVB vessels (r<sup>2</sup> = 0.03, 0.04; p = 0.04, 0.02, respectively), and PSV of left NVB vessels. PSV of bilateral NVB vessels were associated with the storage score (p = 0.022 and p = 0.016), but not with the voiding score. The sum of the frequency and urgency score was also associated with EDV of both capsular and urethral branches (p = 0.043 and p = 0.009, respectively), and PSV of NVB vessels on both sides (p = 0.045 and p = 0.019, respectively). <b><i>Conclusions:</i></b> There is an association between PBF and LUTS, especially with storage symptoms. The findings may provide some insights in understanding the underlying pathophysiology of lower urinary tract dysfunction.
<i>Objectives:</i> To describe and compare primary urethral carcinomas in South Taiwan with those in the USA and to explore the influence of chronic arsenic exposure. <i>Methods:</i> From 1988 to 2001, there were 21 pathologically proven primary urethral carcinomas diagnosed and treated at our hospital (14 males, 7 females). Seven of 14 male patients were chronically exposed to arsenic in drinking water for an average of 23 years. We compared our cases to three studies in the USA (80 males, 179 females), and analyzed the influence of chronic arsenic exposure by onset age, histology, staging, and outcome. <i>Results:</i> Male patients with localized tumors had better survival compared to those with advanced tumors (p = 0.0045 in males, p = 0.07 in females). In comparison to the three studies in the USA, there was an unusual higher frequency of bulbomembranous adenocarcinoma at our center (43 vs. 18%, 2 and 0%, respectively, p < 0.0001), particularly among those with chronic arsenic exposure (73 vs. 14%, p = 0.031). <i>Conclusions:</i> In South Taiwan, there was a high frequency of bulbomembranous urethral adenocarcinoma, which might be associated with chronic arsenic exposure. Although the implications of such an observation are minimal owing to its rarity, it is worth exploring.
Prothymosin‐α ( PTMA ) is a small, acidic protein that is usually transported into the nucleus and involves many cellular and immunological functions. Previous studies demonstrated that aberrant location of PTMA expression exists in human bladder cancer, but the role of PTMA protein expression remains elusive. In this study, we created ectopic nuclear or cytoplasmic PTMA expression in human bladder cancer cells by infecting lentiviruses carrying wild type or deleted nuclear localization signal of the PTMA gene. The in vivo tumorigenesis assay showed PTMA protein with deleted nuclear localization signal promotes J82 xenograft tumor growth in mice and shortens their survival more so than the wild type. Chromatin immunoprecipitation showed that wild‐type PTMA protein binds to the PTEN promoter and enhances phosphatase and tensin homolog ( PTEN ) expression. Through immunoblot proteomics and in vivo ubiquitination studies, PTMA protein can bind with tripartite motif‐containing protein 21 ( TRIM 21) and block its ubiquitination. Also, TRIM 21 can downregulate both forms of PTMA protein. In human bladder tumors, loss of nuclear PTMA expression was an unfavorable prognostic indicator for shorter disease‐free survival (hazard ratio, 1.54; P = 0.009). Our data support that nuclear PTMA protein serves as a tumor suppressor in bladder cancer through upregulating PTEN and orchestrating TRIM 21 for the regulation of Nrf2 signaling.
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